Internal Medicine Emergency Lecture Series Cardiovascular Emergencies July 12, 2004 Scott Chapman, MD

Introduction Review of cardiovascular emergencies – Acute Coronary Syndromes STEMI UA/NSTEMI

– Congestive Heart Failure – Aortic dissection – Digoxin toxicity – Tamponade

Acute Coronary Syndromes ACS - Spectrum of the same disease ST Elevation Myocardial Infarction (STEMI) NonNon-ST Elevation Myocardial Infarction (NSTEMI) Unstable Angina (UA)

Summary and Questions

What do you do when your patient has chest pain? Ask the nurse what she/he would do in this situation Give the nurse your supervisor’ supervisor’s pager # Order EKG, ASA, NTG, betabeta-blockers, heparin, Integrilin, morphine, and thrombolytics (just to be safe) Go home sick because you now have chest pain Take a deep breath and think

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Atherosclerotic Lesions Arterial Disease Progression

Pathophysiology Plaque fissure and rupture Vessel occlusion – fibrin, platelet aggregates, red blood cells Other causes – Dynamic obstruction – Progressive mechanical obstruction – Inflammation/infection – Secondary unstable angina (blood loss, SVT, hypotension, thyrotoxicosis, etc.)

Fatty Streak

Fibrous Plaque

Intermediate Lesion

Plaque Rupture - Advanced Lesion

STEMI About 1.5 million patients have AMI in U.S. each year In U.S. CAD costs more than $60 billion/yr Large indirect cost due to lost productivity Death rate has dropped over last 15 years, but still about 30 percent mortality. 50% of deaths due to AMI occur within 1 hour of event (mostly due to arrhythmias) About 6% mortality for those arriving in hospital treated with thrombolytics NEJM 342:2:101-114

Aspects of MI by Different Techniques Pathology

Myocardial cell death

Biochemistry

Serum markers of myocardial cell death

EKG

Evidence of myocardial ischemia (ST-T wave changes Evidence of loss of electrically active cardiac tissue (Q waves)

Imaging

Reduction or loss of tissue perfusion Cardiac wall motion abnormalities

Differential Diagnosis of STST-Segment Elevation Acute myocardial infarction Post MI aneurysm Acute pericarditis Normal variant LVH/LBBB (usually in V1-2 or V3) Myocarditis Tumor invading LV

Alpert and Thygesen, etal, Myocardial Infarction Redefined JACC Vol. 36, No. 3, September 2000:959–69

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Differential Diagnosis of STST-Segment Elevation Trauma to LV Hypothermia/Osborne waves After DCCV Intracranial hemorrhage Hyperkalemia or hypercalcemia Brugada pattern Type IC antiarrhythmics J-pt. elevation

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STEMI Options for therapy – Thrombolytics – Primary Percutaneous Intervention

GISSI, TIMI, TAMI, ASSENT, MITI, GUSTO, LATE, ISIS, SPEED, DANAMI, InTIME, INJECT, RAPID, COMPASS, SHOCK, etc… etc… Currently first line treatment at UNMC and the VA is thrombolytics unless contraindications

STEMI Absolute contraindications to thrombolytics – Active internal bleeding – Suspected Aortic dissection – Recent head trauma or known intracranial tumor – History of hemorrhagic CVA or cerebrovascular event within 1 year – Major surgery or trauma < 2 wks prior

STEMI Age > 75 – Risk is high with or without therapy. Advantage is less in this age group, but still have 10 lives saved per 1000 treated

STEMI Indications for thrombolytics – Chest pain consistent with AMI – EKG – ST elevation > 0.1mV in 2 contiguous leads or presumed new LBBB – Cardiac enzyme elevation – < 6 hrs – most benefit – 6-12 hrs – still beneficial – > 12 hrs diminishing benefit, may be useful for selected patients

STEMI Relative contraindications to thrombolytics – – – – – – – – – –

BP > 180/100 on 2 readings H/O chronic severe HTN Active PUD H/O CVA or intracerebral pathology not covered in contraindications Known bleeding diathesis or on therapeutic doses of coumadin (INR 2 – 3) Prolonged traumatic CPR or recent trauma (2 to 4 weeks) Recent (2 to 4 weeks) internal bleeding Pregnancy Prior streptokinase/anistreplase within 2 years Noncompressible vascular punctures

STEMI Time is muscle Infarct size is important in prognosis – Larger area of infarct leads to decreased EF – Mortality is higher with larger area of infarction

Desired doordoor-toto-drug time is < 30 minutes General concepts – Open artery early – Reduce myocardial energy requirements (i.e. beta blockers, lower blood pressure, ensure adequate oxygenation)

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Lives saved per 1000 treated

Time and Thrombolytics

Other therapies

35

35 30

25

25

19

20

16

15 10 5 0 0-1 hour

STEMI

2-3 hours

4-6 hours

7-12 hours

Time to treatment from symptom onset

– ASA – Heparin - UFH or LMWH – Beta blockers as tolerated (i.e. metoprolol 5mg IV q 15 min X 3) – NTG – Morphine – Oxygen – Monitor rhythm, vitals closely – ACEACE-I for reduced LVEF – HMG CoCo-A reductase inhibitors during hospitalization

Complications of STEMI Cardiogenic shock – Occurs in about 10% of all AMI – 80% fatal with conservative management – PCI (percutaneous intervention) is primary treatment – May need IABP (intra(intra-aortic balloon pump), inotropes, fluids

Complications of STEMI Heart Block – Anterior MI Causes damage to infrainfra-nodal conduction system With 2nd degree AVB need to pace at early stage because may rapidly change to 3rd degree block

– Inferior MI May cause heart block because of activation of cardiovascular reflexes or due to injury to AVN. Usually pace heart block for symptoms of hypoperfusion

Complications of STEMI Ventricular rupture – – –

Ventricular free wall Ventricular septum Treatment is emergency cardiac surgery

Acute Mitral Regurgitation – Papillary rupture or ischemia May present up to 1 week after AMI Murmur variable

– MV annular dilatation from LV failure – Echocardiography is test of choice – Therapy is urgent cardiac surgery

NSTEMI/UA UA – Rest angina – NewNew-onset severe angina – Accelerating symptoms

NSTEMI UA + biochemical markers (troponins) Risk Assessment – – – –

History Physical Exam X-ray Laboratory

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NSTEMI/UA TIMI Risk Score – Age > 65 – More than 3 coronary risk factors – Prior angiographic coronary obstruction – STST-segment deviation – > 2 anginal events in past 24 hours – Use of ASA within last 7 days – Positive cardiac serum markers

Medical Management Aspirin Nitroglycerin Heparin GP IIb/IIIa inhibitors Beta blockers HMG CoCo-A reductase inhibitors Clopidogrel RISC, TIMI, ATACS, FRISC,CATURE,OASIS, PRISM, VANQWISH, ESSENCE, PURSUIT, PARAGON, ESSENCE, etc...

NSTEMI/UA TIMI Risk Score – Risk of adverse outcome (death, reinfarction, or recurrent ischemia requiring revascularization) 5% with TIMI Risk Score of 0 or 1 41% with TIMI Risk Score of 6 or 7

Guidelines for Classification Class I – Conditions for which there is evidence and/or general agreement that a given procedure/therapy is useful and effective

Class II – Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of performing the procedure/therapy

Class IIa – Weight of evidence/opinion is in favor of procedure/therapy

Class IIb – Usefulness/efficacy is less well established by evidence/opinion

Class III – Conditions for which there is evidence and/or general agreement that a procedure/therapy is not useful and in some cases harmful

Aspirin Irreversibly inhibits cycloxygenase preventing synthesis of thromboxane A2 Class I indications – ASAP upon admission unless intolerance

30% to 40% nonresponders in pts with ACS

Clopidogrel Class I indications: – Hospitalized patients unable to take ASA due to hypersensitivity or major GI bleed – Hospitalized patients to undergo early noninterventional approach – In patients for whom PCI is planned and are not at high risk for bleeding

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Clopidogrel

Glycoprotein IIb/IIIa Inhibitors Class I Indications

CURE trial – 12,562 ACS (UA/NSTEMI) patients. ASA vs. ASA + clopidogrel – 3 to 12 month follow up – Composite endpoint of CV death, MI, or stroke 11.47% vs. 9.28% p = 0.00005 – No significant difference in CV death, refractory ischemia – Significant differences in MI, stroke, inin-hospital refractory ischemia – Very low percentage of patients received IIb/IIIa inhibitors

– In addition to ASA and heparin in patients planned for catheterization and PCI

Class IIa – In addition to ASA and LMWH or UFH in patients with ongoing ischemia, elevated troponin, or with other high risk features in whom invasive management not planned – Patients on heparin, ASA, and clopidogrel in whom cath and PCI are planned

Class IIb – Patients without ongoing ischemia who have no other highhigh-risk features and in whom PCI not planned

Class III – Abciximab in patients whom PCI not planned

10 to 15% of patients with ACS will go to CABG

Low Molecular Weight Heparin

Heparin Class I indication Well established efficacy in ACS Highly variable dosedose-response relationship May be reversed if necessary Short halfhalf-life May stimulate platelet activation Thrombocytopenia is a potential complication

Beta Blockers in ACS Class 1 indication Limited randomized trial data Practice extrapolated from other experience in ischemic syndrome

Class I Indication – In addition to antianti-platelet therapy

Class IIa – Preferable to UFH in the absence of renal failure and unless CABG is planned (Recent JAMA article refutes)

Lower incidence of thrombocytopenia Need to be aware of dose adjustment for renal failure Cannot be reversed

Invasive Therapy Class 1 indication – Recurrent angina/ischemia at rest or with lowlow-level activities despite intensive antianti-ischemic therapy – Elevated troponin – New or presumably new STST-segment depression – Recurrent angina with CHF symptoms, S3, pulmonary edema , worsening rales, worsening MR – HighHigh-risk findings on noninvasive test – Depressed LV systolic function – Hemodynamic instability – Sustained VT – PCI within 6 months – Prior CABG Braunwald et al. 2002, ACC/AHA Practice Guidlines

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Invasive Therapy

Troponin level and mortality

Class IIa indication – Patients with repeated presentations for ACS despite therapy and without evidence for ongoing ischemia or high risk

Class III – Patients with extensive comorbidities in whom risks of revascularization are not likely to outweigh the benefits – Acute chest pain and low likelihood of ACS – Patients not willing to consent to revascularization regardless of findings Braunwald et al. 2002, ACC/AHA Practice Guidlines

Braunwald et al. 2002, ACC/AHA Practice Guidlines

Acute Coronary Syndrome

65 y/o male with a history of anterolateral MI 3 years ago, DM, HTN presents to ER with rapid onset of shortness of breath at 9 PM while while taking garbage out to end of driveway. Squad called and taken to to nearest ER. Currently on 6 l/min via nasal cannula, SpO2 = 87%. Home meds include enalapril, metoprolol, ASA, glyburide, digoxin, digoxin, furosemide

Acute Coronary Syndrome ST Elevation MI Primary PCI/ Thrombolytics

Patient Presentation

UA/ Non-ST Elevation MI Evaluate Risk Factors

Medical Therapy Based on Risk Functional Study vs. Cath

Physical Exam BP210/112 HR 110, RR 24, T37, SpO2 89% Gen: Moderate respiratory distress Neck: JVD 14 cm Heart: Tach regular, + S4 Lungs: Crackles 1/3 of lower lungs b/l Ext: No edema CXR: pulmonary edema with cardiomegaly EKG: Sinus tachycardia with no ST changes Code called in the Unit and your supervisor offers to go to code while you dictate and write orders on this patient.

Acute CHF Common patient presentation: – Shortness of breath, dyspnea on exertion, paroxysmal nocturnal dyspnea, orthopnea, swelling, weight gain – JVD, PND, S3, S4, parasternal lift, crackles, edema, ascites, or hepatomegaly – Pulmonary edema with cardiomegaly on CXR – Elevated BNP (CHF peptide) level, EKG changes depending on etiology

Acute CHF CausesCauses– Ischemia – Complications of MI (i.e. ventricular rupture, arrhythmia, acute MR) – Arrhythmia – high degree AVB, tachyarrhythmia – Tamponade – Pulmonary embolus – Myocarditis – Acute or worsening of valvular lesions – Acute increase in BP – Acute renal failure – Peripartum – Infiltrative diseases – sarcoid, amyloid

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Acute CHF Framingham Criteria for Diagnosis of CHF – Major PND or Orthopnea JVD Rales Cardiomegaly Acute pulmonary edema S3 HJR Circulation time > 25 seconds

Minor Criteria – – – – – – –

Edema Night cough DOE Hepatomegaly Pleural effusion HR > 120 Vital capacity < 1/3 of maximum

Acute CHF Assess the following: – Volume status via Physical Exam, CXR – LV function – Echo – Rule out ischemia – Evaluate for other correctable causes from differential diagnosis

2 major or 1 major and 2 minor criteria for definite CHF

Acute CHF Precipitating Factors – – – – – – – – – –

Noncompliance with diet or medications Arrhythmia Infection Pulmonary embolism Anemia or other high output state CoCo-morbidity such as renal failure, hypothyroidism, lung disease Ischemia Hypertension Alcohol or street drugs Other cardiotoxins such as chemotherapy agents

Aortic Dissection Typical features: – Acute onset of severe pain in chest, back, abdomen – HTN – Aortic diastolic murmur – Pulse deficits – Acute MI from coronary involvement – Syncope from tamponade – CHF from severe AR

Acute CHF Treatment for CHF (Depressed LVEF) – – – – – – – –

Sitting position O2 via any method (NC, mask, BiPap, Ventilator) IV loop diuretics (Lasix, Bumex, etc.) NTG drip MSO4 IV IV nesiritide, dobutamine, milrinone Foley catheter Invasive monitoring - SwanSwan-Ganz catheter, arterial blood pressure line

Aortic Dissection CXR – useful as first screen and may show widening of mediastinum, deviation of mediastinum to the right Definitive diagnosis – TEE – CT angiogram – MRI – Aortography

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Aortic Dissection Surgery for Type I or II (involving the ascending aorta) Initial Treatment – IV betabeta-blockers (propranolol, esmolol, metoprolol, labetalol) – Sodium nitroprusside – Goal SBP of 100 to 120 mmHg or lowest possible to perfuse organs – Reduce HR to about 60 bpm – Watch for acute AI, acute inferior MI, or neurologic changes, acute renal failure, limb ischemia (indicating extension of dissection into other vessels)

Digoxin Toxicity Most common symptoms include: – Nausea, vomiting – Drowsiness

Possible arrhythmias – VT – Sinus bradycardia – Heart block – Paroxysmal atrial tachycardia with block

Digoxin Toxicity If acute, can induce vomiting, perform gastric lavage, and give charcoal DigoxinDigoxin-immune Fab for VT or VF, high grade AV block not responding to atropine, ingestion of high doses, serum level greater than 10ng/ml, or hyperkalemia May cause hyperkalemia – treat same way as isolated hyperkalemia High grade AV block can be treated with atropine and temporary pacing Treat ventricular arrhythmias with lidocaine, phenytoin, esmolol, magnesium, and synchronized DCCV if unstable

Tamponade Clinical findings – Fall in systemic arterial pressure – Rise in systemic venous pressure – Heart sounds distant, possible friction rub – Tachycardia, tachypnea – Pulsus paradoxus (do not send patient down for Echo before you check) – Elevated JVD

Tamponade Etiologies – – – – – – – – – –

Malignancy Idiopathic pericarditis Uremia AMI Iatrogenic (procedures) Infectious/Tuberculosis Radiation Medications SLE Post pericardiotomy

Tamponade Diagnostic studies – EKG Electrical alternans indicating swinging motion of heart May also occur in pericarditis (i.e. not 100% specific)

– CXR May be completely normal unless fluid gradually accumulated (i.e. greater than 250 cc) May have water bottle appearance

– Echocardiogram RA diastolic collapse, RV early diastolic collapse, swinging heart, IVC plethora, Inspiratory decrease in MV inflow pattern

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Tamponade Treatment – Hemodynamic support with IV fluids – Pericardiocentesis – echo or fluoroscopy guided – Pericardiotomy or pericardiectomy

Summary Evaluate the patient Develop a differential Think before you write orders

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